Indigenous tradition and the colonial legacy : a study in the social context of anglophone African literary criticism.

Bibliography: leaves 219-229.This dissertation attempts to examine the social meanings of anglophone African literary criticism as an ideological discourse. It begins by engaging with Marxist critical traditions, with particular reference to two areas of debate: the question of the epistemological relationship between literature and criticism, and the question of criticism's being a discourse which, in its articulation with a given social context, relies on the resources of a particular critical heritage. The basis of the second and central chapter is the interrelationship between the context and heritage of anglophone African criticism. The dominant themes of this discourse are seen as being shaped by ideological affiliations with the modern nation-state, and by the legacy of the empirical and organic traditions of metropolitan criticism. It is argued that in the situation of neo-colonial social stratification, anglophone African criticism faces a crisis of legitimacy. In the third to fifth chapters I attempt to illustrate and refine the central argument in relation to a selection of critical texts. The chapter on two works by Eldred Jones examines his reliance on orthodox British critical assumptions and its consequences in his treatment of the writing of Wole Soyinka. The chapter on West African traditions examines a range of critical operations which are used in the construction of organic traditions based on oral or traditional cultures. These operations rely on mythopoesis, formalism and the sociology of literature. The final chapter on East African political readings investigates the internal, discursive tensions in the work of two critics who, in attempting to politicize their reading of literature, have not been able to achieve a conceptual break from the legacies of idealism

A tight squeeze: How do we make sense of small changes in microvascular diameter?

The brain is an energetically demanding tissue which, to function adequately, requires constant fine tuning of its supporting blood flow, and hence energy supply. Whilst blood flow was traditionally believed to be regulated only by vascular smooth muscle cells on arteries and arterioles supplying the brain, recent work has suggested a critical role for capillary pericytes, which are also contractile. This concept has evoked some controversy, especially over the relative contributions of arterioles and capillaries to the control of cerebral blood flow. Here we outline why pericytes are in a privileged position to control cerebral blood flow. First we discuss the evidence, and fundamental equations, which describe how the small starting diameter of capillaries, compared to upstream arterioles, confers a potentially greater control by capillary pericytes than by arterioles over total cerebral vascular resistance. Then we suggest that the faster time frame over which low branch order capillary pericytes dilate in response to local energy demands provides a niche role for pericytes to regulate blood flow compared to slower responding arterioles. Finally, we discuss the role of pericytes in capillary stalling, whereby pericyte contraction appears to facilitate a transient stall of circulating blood cells, exacerbating the effect of pericytes upon cerebral blood flow

Pericyte-mediated constriction of renal capillaries evokes no-reflow and kidney injury following ischaemia

Acute kidney injury is common, with ~13 million cases and 1.7 million deaths/year worldwide. A major cause is renal ischaemia, typically following cardiac surgery, renal transplant or severe hemorrhage. We examined the cause of the sustained reduction in renal blood flow ('no-reflow'), which exacerbates kidney injury even after an initial cause of compromised blood supply is removed. Adult male Sprague-Dawley rats, or NG2-dsRed male mice were used in this study. After 60 min kidney ischaemia and 30-60 min reperfusion, renal blood flow remained reduced, especially in the medulla, and kidney tubule damage was detected as Kim-1 expression. Constriction of the medullary descending vasa recta and cortical peritubular capillaries occurred near pericyte somata, and led to capillary blockages, yet glomerular arterioles and perfusion were unaffected, implying that the long-lasting decrease of renal blood flow contributing to kidney damage was generated by pericytes. Blocking Rho kinase to decrease pericyte contractility from the start of reperfusion increased the post-ischaemic diameter of the descending vasa recta capillaries at pericytes, reduced the percentage of capillaries that remained blocked, increased medullary blood flow and reduced kidney injury. Thus, post-ischaemic renal no-reflow, contributing to acute kidney injury, reflects pericytes constricting the descending vasa recta and peritubular capillaries. Pericytes are therefore an important therapeutic target for treating acute kidney injury

Fast Removal of Synaptic Glutamate by Postsynaptic Transporters

AbstractGlutamate transporters are believed to remove glutamate from the synaptic cleft only slowly because they cycle slowly. However, we show that when glutamate binds to postsynaptic transporters at the cerebellar climbing fiber synapse, it evokes a conformation change and inward current that reflect glutamate removal from the synaptic cleft within a few milliseconds, a time scale much faster than the overall cycle time. Contrary to present models, glutamate removal does not require binding of an extracellular proton, and the time course of transporter anion conductance activation differs from that of glutamate removal. The charge movement associated with glutamate removal is consistent with the majority of synaptically released glutamate being removed from the synaptic cleft by postsynaptic transporters

The Effect of Hyperoxemia on Neurological Outcomes of Adult Patients: A Systematic Review and Meta-Analysis

Hyperoxemia commonly occurs in clinical practice and is often left untreated. Many studies have shown increased mortality in patients with hyperoxemia, but data on neurological outcome in these patients are conflicting, despite worsened neurological outcome found in preclinical studies. To investigate the association between hyperoxemia and neurological outcome in adult patients, we performed a systematic review and meta-analysis of observational studies. We searched MEDLINE, Embase, Scopus, Web of Science, Cumulative Index to Nursing and Allied Health Literature, and ClinicalTrials.gov from inception to May 2020 for observational studies correlating arterial oxygen partial pressure (PaO2) with neurological status in adults hospitalized with acute conditions. Studies of chronic pulmonary disease or hyperbaric oxygenation were excluded. Relative risks (RRs) were pooled at the study level by using a random-effects model to compare the risk of poor neurological outcome in patients with hyperoxemia and patients without hyperoxemia. Sensitivity and subgroup analyses and assessments of publication bias and risk of bias were performed. Maximum and mean PaO2 in patients with favorable and unfavorable outcomes were compared using standardized mean difference (SMD). Of 6255 records screened, 32 studies were analyzed. Overall, hyperoxemia was significantly associated with an increased risk of poor neurological outcome (RR 1.13, 95% confidence interval [CI] 1.05-1.23, statistical heterogeneity I2 58.8%, 22 studies). The results were robust across sensitivity analyses. Patients with unfavorable outcome also showed a significantly higher maximum PaO2 (SMD 0.17, 95% CI 0.04-0.30, I2 78.4%, 15 studies) and mean PaO2 (SMD 0.25, 95% CI 0.04-0.45, I2 91.0%, 13 studies). These associations were pronounced in patients with subarachnoid hemorrhage (RR 1.34, 95% CI 1.14-1.56) and ischemic stroke (RR 1.41, 95% CI 1.14-1.74), but not in patients with cardiac arrest, traumatic brain injury, or following cardiopulmonary bypass. Hyperoxemia is associated with poor neurological outcome, especially in patients with subarachnoid hemorrhage and ischemic stroke. Although our study cannot establish causality, PaO2 should be monitored closely because hyperoxemia may be associated with worsened patient outcome and consequently affect the patient's quality of life

Why do oligodendrocyte lineage cells express glutamate receptors?

The function of glutamate receptors on oligodendrocytes and their precursor cells is poorly understood, with their only clear action being to damage these cells in pathological conditions. Here we review recent studies of glutamate signalling to oligodendrocyte lineage cells, and explore what its physiological function may be

Duplicando o Escritor: David Attwell sobre seu diálogo textual com J. M. Coetzee

A autora apresenta nessas entrevistas, nas quais ela e David Atwell investigam a natureza da verdade, da realidade e da escrita como interpretada por Coetzee em seu trabalho, cresceram até se tornaram a coleção de ensaios, comentários e diálogos Doubling the Point, de 1992 (algo como Duplicando o Ponto, sem tradução em português). Como todos os leitores de Coetzee devem saber, Doubling the Poing tem sido massivamente influente em moldar as definições e as dimensões do pensamento crítico da obra de Coetzee. Em especial, talvez, em moldar o entendimento crítico da contida auto-reflexão e do envolvimento comprometido com as complexidades da representação, elementos que perpassam todo o trabalho de Coetzee

Hyperoxia evokes pericyte-mediated capillary constriction

Oxygen supplementation is regularly prescribed to patients to treat or prevent hypoxia. However, excess oxygenation can lead to reduced cerebral blood flow (CBF) in healthy subjects and worsen the neurological outcome of critically ill patients. Most studies on the vascular effects of hyperoxia focus on arteries but there is no research on the effects on cerebral capillary pericytes, which are major regulators of CBF. Here, we used bright-field imaging of cerebral capillaries and modeling of CBF to show that hyperoxia (95% superfused O2) led to an increase in intracellular calcium level in pericytes and a significant capillary constriction, sufficient to cause an estimated 25% decrease in CBF. Although hyperoxia is reported to cause vascular smooth muscle cell contraction via generation of reactive oxygen species (ROS), endothelin-1 and 20-HETE, we found that increased cytosolic and mitochondrial ROS levels and endothelin release were not involved in the pericyte-mediated capillary constriction. However, a 20-HETE synthesis blocker greatly reduced the hyperoxia-evoked capillary constriction. Our findings establish pericytes as regulators of CBF in hyperoxia and 20-HETE synthesis as an oxygen sensor in CBF regulation. The results also provide a mechanism by which clinically administered oxygen can lead to a worse neurological outcome

Non-signalling energy use in the developing rat brain

Energy use in the brain constrains its information processing power, but only about half the brain's energy consumption is directly related to information processing. Evidence for which non-signalling processes consume the rest of the brain's energy has been scarce. For the first time, we investigated the energy use of the brain's main non-signalling tasks with a single method. After blocking each non-signalling process, we measured oxygen level changes in juvenile rat brain slices with an oxygen-sensing microelectrode and calculated changes in oxygen consumption throughout the slice using a modified diffusion equation. We found that the turnover of the actin and microtubule cytoskeleton, followed by lipid synthesis, are significant energy drains, contributing 25%, 22% and 18%, respectively, to the rate of oxygen consumption. In contrast, protein synthesis is energetically inexpensive. We assess how these estimates of energy expenditure relate to brain energy use in vivo, and how they might differ in the mature brain